Migraine with aura is caused by a wave of abnormal electrical activity that sweeps across the surface of the brain, temporarily disrupting normal nerve cell function. This wave, called cortical spreading depression, moves slowly at about 2 to 6 millimeters per minute and creates the visual disturbances, tingling, and other sensory symptoms that define an aura. What triggers that wave in the first place involves a combination of genetics, hormones, environmental factors, and brain chemistry that varies from person to person.
The Electrical Wave Behind the Aura
During an aura, a massive wave of nerve cell activation rolls across the brain’s outer layer, followed immediately by a period of electrical silence that lasts several minutes. Think of it like a stadium wave: neurons fire intensely, then go quiet as the wave passes. This wave of depolarization is what produces the strange sensory experiences of an aura, and its slow pace across the brain explains why aura symptoms tend to build and shift gradually over minutes rather than appearing all at once.
The process depends heavily on glutamate, the brain’s primary excitatory chemical messenger. As the wave moves, neurons release glutamate into the space between cells. That released glutamate then triggers neighboring neurons to release even more glutamate, creating a self-sustaining chain reaction. This is why the wave keeps propagating on its own once it starts. Specific receptors on neurons (called NMDA receptors) are critical for igniting and sustaining the wave. When those receptors are blocked in lab experiments, the wave can’t start. Conversely, lowering magnesium levels around brain cells, which effectively unlocks those same receptors, can trigger one.
What Aura Looks and Feels Like
Visual symptoms are the most common type of aura. The classic version is a shimmering, flickering disturbance that often starts near the center of your vision and slowly expands outward. People describe it as looking through a kaleidoscope, or like heat ripples rising off a hot road. The patterns can take several forms: jagged zigzag lines (sometimes called fortification patterns because they resemble the notched top of a castle wall), rings or crescent-shaped arcs, or even checkerboard-like squares. These visual disturbances are fully reversible and typically last between 5 and 60 minutes.
Sensory aura is the second most common type. It usually begins as tingling or numbness in one hand, then slowly marches up the arm over 5 to 10 minutes. In about two-thirds of cases, it jumps to the same side of the face. Tingling of the tongue is particularly characteristic of migraine and is actually the most common cause of episodic tongue numbness. Some people also experience speech difficulties during an aura, struggling to find words or slurring their speech. These symptoms can occur alone or in sequence with visual changes, and when multiple aura symptoms happen in succession, the entire episode can last longer, up to 60 minutes per symptom type.
Genetics and Brain Excitability
Migraine with aura runs in families, and research into rare inherited forms of migraine has revealed why. Three genes identified so far all control ion channels and pumps that regulate how excitable your brain cells are. Mutations in a gene called CACNA1A create overactive calcium channels that cause neurons to release too much glutamate. Mutations in ATP1A2 impair a pump that normally clears glutamate away from the gaps between neurons, letting it accumulate. And mutations in SCN1A make sodium channels overactive, leading to excessive nerve cell firing.
All three mutations point to the same core problem: a brain that tips too easily into the runaway electrical excitation that launches cortical spreading depression. These specific gene variants cause a severe inherited form of migraine, but they illustrate the broader principle at work in common migraine with aura. People who experience aura likely have some degree of heightened cortical excitability, whether from identified genetic variants or from subtler inherited traits that make their neurons more prone to that chain reaction of glutamate release.
Hormonal Triggers
The drop in estrogen that happens just before menstruation is one of the most well-established migraine triggers. First proposed in 1972, the estrogen withdrawal hypothesis holds that it’s not low estrogen itself that causes problems, but the sharp decline after a prolonged period of high levels. Research supports this: in studies where women were given estrogen supplements and then taken off them, migraine frequency increased by about 40% in the five days after withdrawal compared to placebo.
This hormonal connection helps explain why migraine with aura disproportionately affects women during their reproductive years and why attacks often cluster around menstruation, the postpartum period, and the transition to menopause. Some evidence suggests estrogen withdrawal increases pain sensitivity and may also lower the threshold for that cortical spreading depression wave, making the brain more susceptible to aura.
Environmental and Lifestyle Triggers
A wide range of external factors can push a susceptible brain past the threshold for an aura. Weather-related triggers are among the most commonly reported: bright sunlight, sun glare, extreme heat or cold, high humidity, dry air, windy or stormy weather, and changes in barometric pressure. These triggers don’t cause migraine on their own. They act on a brain that’s already genetically primed for heightened excitability, nudging it past the tipping point.
Other well-known triggers include sleep disruption (too little or too much), skipped meals, dehydration, stress or the letdown period after stress, strong smells, and certain foods. Most people with migraine have multiple triggers, and attacks often happen when several converge. You might tolerate bright sunlight on a well-rested day but not when you’re also dehydrated and stressed.
A Heart Defect That May Play a Role
A surprisingly high number of people with migraine with aura have a small hole between the upper chambers of their heart called a patent foramen ovale, or PFO. Everyone is born with this opening, but it normally closes shortly after birth. In the general population, roughly 25% of people retain a small PFO. Among people with migraine with aura, that number jumps to between 46% and 88%, compared to 16% to 35% in people who have migraine without aura.
The leading theory is that a PFO allows tiny blood clots or chemical signals that would normally be filtered by the lungs to pass directly into the arterial circulation and reach the brain, potentially triggering cortical spreading depression. The relationship is still not fully understood, and closing the PFO surgically has shown mixed results for reducing migraine, so the connection is likely more complex than a simple cause-and-effect.
Why Aura Raises Stroke Risk
People who have migraine with aura face roughly double the risk of ischemic stroke compared to people without migraine. Importantly, migraine without aura does not carry the same elevated risk. The mechanism isn’t entirely clear, but the cortical spreading depression wave itself may contribute by temporarily reducing blood flow in affected brain regions. Over time, repeated episodes could contribute to small changes in blood vessel function. This elevated risk is one reason doctors consider aura status when making decisions about prescribing estrogen-containing birth control, which carries its own small stroke risk.
The absolute risk remains low for most people. Doubling a very small number still produces a small number. But the association is strongest in women under 45 who smoke and use estrogen-containing contraceptives, where the combination of risk factors becomes more meaningful.